Congestive heart failure (CHF) is a clinical syndrome in which an abnormality of cardiac function causes cardiac output to fall below a level adequate to meet the metabolic demand of peripheral tissues. CHF can be due to a variety of etiologies with that due to ischemic heart disease being the most common. The most common way of treating CHF is drug therapy, but recent studies have demonstrated that some CHF patients may benefit from cardiac pacing therapy. Some CHF patients suffer from bradycardia, a traditional indication for cardiac pacing, but others exhibit a delay in ventricular contraction which leads to inadequate filling during diastole and decreased cardiac output. Such ventricular contraction delays can be due to some degree of AV block, and cardiac output in those patients can be improved by synchronizing atrial and ventricular contractions with dual-chamber pacing using a short programmed AV delay time. It has also been shown that some CHF patients suffer from intraventricular conduction defects (a.k.a. bundle branch blocks) such that their cardiac outputs can be increased by improving the synchronization of ventricular contractions. Ventricular synchrony can be improved either by pacing one ventricle or providing pacing to both ventricles separately, termed biventricular pacing.
The normal rhythmic impulse of the heart is first generated in pacemaker tissue known as the sino-atrial (SA) node, spreads throughout the atria causing atrial contraction, and is then conducted to the atrioventricular (AV) node where the impulse is delayed before passing into the ventricles. The ventricles of a normal heart are then electrically stimulated by excitation emanating from the AV node that spreads to the heart via specialized conduction pathways known as Purkinje fibers. The Purkinje system begins from the AV node as the bundle of His and then divides into right and left bundle branches to supply excitation to the right and left ventricles. The fibers lie beneath the endocardium and spread throughout each ventricular chamber where they penetrate into the myocardium and become continuous with the muscle fibers. The conduction velocity of the Purkinje fibers is very rapid so that the time between the impulse leaving the AV node and spreading to the entire endocardial surface of the ventricles is only approximately 0.03 seconds. Once the impulse has reached the ends of the Purkinje fibers, it is then transmitted through the ventricular muscle mass by the muscle fibers themselves with a conduction velocity only about one-sixth that of the Purkinje fibers. Because of the rapid excitation of the entire endocardial surface by the Purkinje system, however, the spread of excitation from the endocardial surface to the epicardial surface of the ventricles takes only about another 0.03 seconds. This means that in the normal heart, excitation of the first ventricular muscle fiber occurs only about 0.06 seconds before the last ventricular muscle fiber is excited. The result is a synchronous contraction in which all portions of the ventricular muscle in both ventricles begin contracting at nearly the same time.
Conventional cardiac pacing with implanted pacemakers involves electrical stimulation of the heart by an electrode in electrical contact with the myocardium. The pacemaker is usually implanted subcutaneously on the patient's chest, and is connected to an electrode for each paced heart chamber by leads threaded through the vessels of the upper venous system into the right heart and through the coronary sinus into the left heart. In response to sensed electrical cardiac events and elapsed time intervals, the pacemaker delivers to the myocardium a depolarizing voltage pulse of sufficient magnitude and duration to cause an action potential. A wave of depolarizing excitation then propagates through the myocardium, resulting in a heartbeat.
As noted above, some CHF patients suffer from defects of the Purkinje conduction system such as bundle branch block. Artificial ventricular pacing with an electrode fixed into an area of the myocardium does not use the heart's Purkinje conduction system because that system can only be entered by impulses emanating from the AV node. With pacing, the spread of excitation proceeds from the pacing electrode via the ventricular muscle fibers, thus bypassing the deficient conduction pathway in the CHF patient with bundle branch block and improving cardiac function. If the conduction system is normal or near-normal, however, such pacing can actually worsen cardiac function because the conduction velocity of muscle fibers is much less than that of Purkinje fibers. As pacing therapy continues in a CHF patient over time, a compensatory remodeling process can be expected to occur as the heart adapts to the benefit received from the chronic pacing. Such remodeling may partially regenerate the deficient conduction system. If such is the case, pacing therapy should be adjusted accordingly in order to maintain optimal cardiac function by, e.g., changing the AV delay time or possibly even discontinuing pacing. It would be advantageous in a CHF patient treated with pacing therapy, therefore, if changes in the condition of the heart's conduction system could be ascertained and monitored throughout the course of the therapy.